Using cultured human lymphoid cell lines from selected normal healthy donors and chronic lymphocytic leukemia (CLL) patients we propose to investigate the extent to which expression of HL-A antigens is a function of the cell life cycle. Established lymphoid cell cultures will be snychronized in various cell cycle phases by double-thymidine blocking techniques and by thymidine-colcemid methods of arrest. Respective peripheral lymphocyte suspensions and synchronized cultured lymphoid cell lines will be typed for all presently defined HL-A antigens, by the standard N.I.H. microlymphocytotoxicity method and by absorption of known HL-A antisera with these cells. The essential question here addressed concerns whether human leukemic cells are able to demonstrate a differential expression of their histocompatibility antigens as a function of the various cell cycle phases. It now appears that such phenomena occur in known histocompatibility and tumor antigen systems in mice. If functional expression of cell surface histocompatibility antigens can indeed vary with the cell life cycle, then the fundamental questions raised are those concerned with the extent to which tumor cells are able to 'adapt' or modify their cell cycle characteristics as a means of escaping host immunologic detection or destruction, and how this system might be altered to the disadvantage of the tumor.